The cancer patient exhibits a significant weight loss, primarily due to a loss of skeletal muscle protein, resulting in compromised immune function, multiple organ failure and death. While nutritional support would appear to be the ideal therapy for cancer patients, data indicate minimal positive impact on skeletal muscle protein. These data suggest that the tumor-bearing (TB) host is unable to optimize utilization of exogenous nutrients. One factor having the potential to mediate such a problem is an alteration in intermediary metabolism of lipid. Alterations in lipid metabolism have been reported in clinical and experimental studies. Such reports present a picture of a catabolic state in which, unlike starvation, skeletal muscle protein stores are not protected by a switch from a carbohydrate to a lipid fuel economy. It is hypothesized that one of the primary mediators of cancer cachexia is an inability of skeletal muscle to optimize the utilization of fatty acids as energy sources. This research is designed to delineate this problem using a rat methylcholanthrene sarcoma model. Initial studies are proposed to investigate the efficacy of two treatments on skeletal muscle protein content, tumor growth and immune function. These studies will examine the effect of (1) enteral nutrition, with the traditional and ineffective long-chain triglyceride component switched to the more "anabolically effective" fish oil and medium-chain triglyceride, and (2) the impact of concomitant administration of the anabolically active beta2-adrenergic agonist, cimaterol. It is hypothesized that these treatments will benefit the TB host by promoting a shift from carbohydrate to fat utilization. It is also proposed that this hypothesis be investigated in a series of experiments in which specific in vivo and in vitro indices of skeletal muscle lipid utilization and oxidation are investigated in TB rats that have received the, two types of lipid. It is anticipated that these studies will aid in formulating new and more effective treatment options for the cachectic cancer patient and increase our understanding of mechanisms mediating the development of cancer cachexia.